EDITORIALS Arsenic Trioxide, a Novel Mitochondriotoxic

During the last few years, it has become increasingly clear that mitochondria play a major rate-limiting role in apoptosis (1–3). In general terms, the apoptotic process can be subdivided into three phases: the initiation phase, the decision/effector phase, and the degradation phase. During the heterogeneous ini-tiation phase, which is essentially premitochondrial, specific pro-apoptotic signal transduction pathways or nonspecific dam-age pathways are activated. These pathways converge on the mitochondria during the decision/effector phase, where they trigger progressive permeabilization of mitochondrial mem-branes, mostly as a result of the action of the permeability tran-sition pore complex (PTPC). Thus, the mitochondrion (or to be more precise, the PTPC, which interacts with the Bcl-2/Bax complex) “decides ” the cell’s fate and determines the point of no return of the process (4,5). The morphologic and biochemica